Internet of Things (IoT) is driving the development of new generation of sensors, communication components, and power sources. Ideally, IoT sensors and communication components are expected to be powered by sustainable energy source freely available in the environment. Here, we provide a breakthrough in this direction by demonstrating high output power energy harvesting from very low amplitude stray magnetic field, which exists everywhere, through magnetoelectric (ME) coupled magneto-mechano-electric (MME) energy conversion. ME coupled MME harvester comprised of multiple layers of amorphous magnetostrictive material, piezoelectric macro-fiber composite (MFC), and magnetic tip mass, interacts with external magnetic field to generate electrical energy. Comprehensive experimental investigation and theoretical model reveal that both magnetic torque generated through magnetic loading and amplification of magneto-mechanical vibration by ME coupling contribute towards the generation of high electrical power from the stray magnetic field around power cable of common home appliances. The generated electrical power from the harvester was sufficient for operating micro-sensors (gyro, temperature, and humidity sensing) and wireless data transmission system. These results will facilitate the deployment of IoT devices in emerging intelligent infrastructures.

A magnetoelectric coupled magneto-mechano-electric energy conversion mechanism allows the generation of high electrical power from ambient stray magnetic fields around infrastructures.

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SummaryThe functional effect of the interaction of E2F1 and hepatitis B virus X protein (HBx) on the promoter of human p53 gene was studied using chloramphenicol acetyl transferase (CAT) assay. E2F1 activated the p53 promoter through E2F1 binding site. As previously reported, HBx repressed the p53 promoter through E-box. When E2F1 was cotransfected with HBx, E2F1 overcame the repressive effect of HBx on the p53 promoter through the E2F1 site.

III, Retrospective comparative study.

The switch to an angiogenic phenotype is known to be a fundamental determinant of neoplastic growth and tumor progression. We herein report that the transcription of the human p53 gene was repressed by treatment with a hypoxia-mimicking concentration of cobalt chloride and alone by hypoxia-inducible factor 1K K. Analyses of serial deletions, site-directed mutageneses and heterologous promoter systems showed that the site responsible for the repression by both factors was the E-box element in the promoter of the p53 gene. These results alongside previous data suggest that the loss of p53 including the transcriptional repression may play an important role in the angiogenic switch during tumorigenesis. ß 2001 Published by Elsevier Science B.V. on behalf of the Federation of European Biochemical Societies.